The general objective of this research is to further elaborate the potential significance of psychological stress in the etiology of essential hypertension. A related aim seeks to ascertain whether operant conditioning (biofeedback) of heart rate or oxygen consumption can selectively mitigate or attenuate the cardiovascular response to acute-experimental psychological stress. Three sets of related experiments are proposed which are designed to: (1) evaluate autonomic (sympathetic and vagal) mediation of cardiovascular changes during psychological stress, (2) contrast the hemodynamic-metabolic concomitants of physical (exercise) and behavioral stress and (3) examine whether operant modification of heart rate or oxygen utilization can modify the cardiovascular and metabolic adjustments engendered by psychological stress. These objectives would seem especially justified in light of accumulating evidence implicating autonomically mediated elevations in cardiac output (primary due to heart rate) in the production of appreciable arterial blood pressure increases during psychological stress as well as in the symptomotology of labile or borderline hypertension. The precise metabolic significance of such an elevated cardiac output and heart rate has not been clarified whereas, it is well recognized that comparable adjustments during exercise stress facilitates tissue perfusion in response to an increased demand for oxygen delivery. The major interest of this proposal is whether a similar relationship characterizes the cardiovascular-metabolic response to psychological stress and if operant control procedures can effectively modify this stress response.